Correlation between echocardiographically demonstrated segmental dyskinesis and regional myocardial perfusion.
Author(s) -
Richard E. Kerber,
Melvin L. Marcus,
James C. Ehrhardt,
Robert Wilson,
François M. Abboud
Publication year - 1975
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.52.6.1097
Subject(s) - medicine , perfusion , cardiology , coronary occlusion , occlusion , ischemia , isometric exercise , circumflex , ultrasound , artery , radiology
In order to evaluate the relationship between regional myocardial perfusion and segmental dyskinesis, 22 open chest dogs were studied using ultrasound to register cardiac wall motion and radioactive labeled microspheres to determine myocardial perfusion. In six dogs, motion and perfusion were correlated at two levels of partial circumflex coronary artery occlusion followed by complete occlusion. A good correlation between declining myocardial perfusion of all the ischemic segments and development of aneurysmal bulging (during isometric contraction) was seen: r = minus 0.80. A similar correlation between myocardial perfusion and endocardial wall velocity (during systolic ejection) was observed: r = 0.92. In nine dogs, the effect of 45 minutes of complete coronary occlusion followed by 30 minutes of reperfusion was evaluated with respect to perfusion and motion. After coronary reperfusion myocardial perfusion of the ischemic area returned to control levels (from 32.6 +/- 3.5 to 130.3 +/- 13.3 ml/100 g/min), but aneurysmal bulging during isometric contraction persisted. Endocardial wall velocity during systolic ejection showed a variable response to reperfusion, achieving values ranging from 32% to 162% of the preocclusion levels. In seven dogs the ultrasound beam was reflected off nonischemic myocardium adjacent to areas of ischemia resulting from coronary occlusion. Despite preservation of normal myocardial perfusion in these nonischemic areas wall motion abnormalities were evident: endocardial wall velocity declined from 25.8 +/- 5.8 to 14.0 +/- 4.9 mm/sec (P less than 0.01), and aneurysmal bulging in three animals. These changes may be due to transient undetected ischemia in the segments struck by the ultrasound beam, or to passive alteration of the motion of the normally perfused areas by the severe dyskinesis of the adjacent ischemic myocardium.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom